Background:Аnkylosing spondylitis (AS) and inflammatory bowel diseases (IBD) have many common features. Approximately one in two patients with axial spondyloarthritis have subclinical (histologically confirmed) inflammation of the intestine, and 5-10% of subclinical inflammation turns into Crohn’s disease (CD) or Ulcerative colitis (UC) [1]. Colonoscopy is usually used to diagnose IBD, but this procedure is invasive. Laboratory biomarkers, as fecal calprotectin (FC) and serum calprotectin (SC) can used to diagnosis of IBD. But there is no consensus regarding SC clinical utility. SC is exposed to proteolytic enzymes, but its level also increases with inflammation in the intestine and is associated with a higher disease activity [2]. SC levels positively correlate with CRP, ESR, disease activity in AS, but not as obvious as with FC [3,4].Objectives:The aim of this study was to evaluate the possibility of using SC in the diagnosis of IBD in patients with AS.Methods:In the analysis were included 50 patients with AS, fulfilling the modified New York criteria, among them man -36 (72%), woman -14 (28%), mean age of patients was 42.5 ±9.9, mean disease duration – 13.4±8.7 years. All patients were examined with ESR, CRP, FC (range: 100-1800 µg /g), esophagogastroduodenoscopy, colonoscopy and quantitative analysis of the SC level using ELISA (BUHLMANN MRP8/14 ELISA, range: 0.4-3.9 µg /ml).Results:All patients had a high disease activity, mean BASDAI was 5.3 ± 1.8, mean ASDAS CRP 3.7 ± 1.01, mean ASDAS ESR 3.6 ± 1.01. 80 % patients had high FC level (more than 100 µg / g), while only 18% patients had an increase of SC level. IBD were diagnosed in 11 cases: 6 patients (12 %) with CD and 5 patients (10 %) - UC, in the remaining cases (78%) was no intestinal pathology. Only 2 patients with IBD had a high SC level. SC level was more correlated with ESR (r=0.5) and CRP (r=0.5) (p <0.05) levels, than with FC level (r=0.4) (p <0.05).Conclusion:The results showed that there is currently insufficient data to assess the possibility of using SC in the diagnosis of IBD in patients with AS. There is a significant association between the SC, CRP and ESR, but not fecal calprotectin. Potentially SC may be more representative of systemic inflammation than an intestinal inflammation.References:[1]Klingberg, E., Strid, H., Stahl, A.et al. A longitudinal study of fecal calprotectin and the development of inflammatory bowel disease in ankylosing spondylitis. A longitudinal study of fecal calprotectin and the development of inflammatory bowel disease in ankylosing spondylitis. Arthritis Res Ther 2017. 19(1):21[2]Kalla R, Kennedy NA, Ventham NT, Boyapati RK, Adams AT, Nimmo ER, Visconti MR, Drummond H, Ho GT, Pattenden RJ, Wilson DC, Satsangi J. Serum Calprotectin: A Novel Diagnostic and Prognostic Marker in Inflammatory Bowel Diseases. Am J Gastroenterol. 2016 Dec;111(12):1796-1805[3]Hu H, Du F, Zhang S, Zhang W. Serum calprotectin correlates with risk and disease severity of ankylosing spondylitis and its change during first month might predict favorable response to treatment. Mod Rheumatol. 2019 Sep;29(5):836-842.[4]Azramezani Kopi T, Shahrokh S, Mirzaei S, Asadzadeh Aghdaei H, Amini Kadijani A. The role of serum calprotectin as a novel biomarker in inflammatory bowel diseases: a review study. Gastroenterol Hepatol Bed Bench. 2019;12(3):183-189.Disclosure of Interests:None declared.

Background:Ankylosing spondylitis (AS) is a chronic inflammatory disease of the spine and sacroiliac joints characterized by new bone formation (syndesmophytes) and ankyloses. In AS cases, along with the damage to the musculoskeletal system, impairment of other organs and systems is often observed (uveitis, inflammatory bowel and heart diseases). Pro-inflammatory cytokines (TNF-α, IL-6,-17,-23,-21,-22,-31) and chemokines (IL-8) are key pathogenic markers in AS.Objectives:The aims of the study were to determine the serum levels of IL-6 and IL-8 in AS and investigate their relationship with disease activity.Methods:We studied 140 patients (pts) with AS fulfilled modified New York criteria (1984); (102M/38F); median and interquartile range (25th—75th percentile) of age 43.0; 35.0-51.0 years; disease duration 6.0; 4.0-12.0 years; BASDAI - 5.4; 4.1-6.6; ASDAS ESR - 3.6; 2.6-4.4; ASDAS CRP - 3.8; 2.7-4.5; 86% HLA-27 positive. In 50% of pts with AS, inflammatory bowel diseases (IBD) (Crohn’s disease and ulcerative colitis) were diagnosed. The control group included 17 healthy donors (HC). The serum concentrations of IL-6 and IL-8 were detected by chemiluminescence immunoassay using IMMULATE 1000 analyzer (Siemens Healthcare Diagnostics, USA).Results:AS pts had significantly higher serum level of IL-6 than HC (4.3; 0.1-8.0 pg/ml vs 2.3; 0.1-2.7 pg/ml, p <0.006). The median concentration of IL-8 didn’t differ between AS pts and HC (10.5; 8.3-18.0 pg/ml vs 11.9; 8.2-18.3 pg/ml, p>0.05). The same levels of IL-6 and IL-8 were detected in AS with IBD and AS without signs of IBD (p>0.05). In AS pts, serum IL-6 concentration was positively correlated with ASDAS ESR (r = 0.3), ASDAS CRP (r = 0.3), ESR (r = 0.3) and CRP (r = 0.5) (p <0.05); IL-8 was negatively associated with presence of fecal calprotectin (r = -0.3) (p <0.05).Conclusion:Elevated serum concentration of IL-6 in AS is associated with clinical and laboratory markers of high inflammatory activity of the disease. The levels of IL-8 in the sera of AS patients were negatively correlated with the concentration of fecal calprotectin. Data on the relationship of IL-8 with the activity of the pathological process in AS require further study.Disclosure of Interests:Elena Aleksandrova: None declared, Alexander Novikov: None declared, Polina Kulakova: None declared, Aleksey Dorofeev: None declared, Nadezhda Savenkova: None declared, Evgeniy Volnukhin: None declared, Anton Kovshik: None declared, Galina Lukina Speakers bureau: Novartis, Pfizer, UCB, Abbvie, Biocad, MSD, Roche

Background. Аnkylosing spondylitis (AS) is closely associated with inflammatory bowel disease (IBD). 5–10 % of patients with SpA eventually develop inflammatory bowel disease, with Crohn's disease being more common than ulcerative colitis. Colonoscopy is usually used to diagnose inflammatory bowel disease, but this procedure is invasive. FC is clinically used to detect IBD and correlates well with clinical, endoscopic, and histological indicators of disease activity in IBD.The aim. To evaluate the incidence of inflammatory bowel disease in patients with ankylosing spondylitis.Materials and methods. In the analysis were included 40 patients with ankylosing spondylitis, among them 26 (65.0 %) men, and 14 (35.0 %) women, the average age of patients was 41.2 ± 10.5, the duration of the disease was on average 13.0 ± 8.8 years. All patients were examined with ESR, CRP, esophagogastroduodenoscopy, colonoscopy and quantitative analysis of the fecal calprotectin levels using the method of lateral immunochromatography with the BUHLMANN Quantum Blue rapid test. Standart range: 100–1,800 µg/g.Results. All patients had a high disease activity, the average BASDAI was 5.2 ± 1.7, the average ASDAS CRP 3.8 ± 1.1. 35 (87.5 %) patients had calprotectin level more than 100 µg/g, the remaining 5 (12.5 %) patients less than 100 µg/g. 12 (30.0 %) patients had the calprotectin level more than 1,800 µg/g, 23 (57.5 %) from 101 to 1800 µg/g. All patients with FC levels more than 100 µg/g showed an increase CRP level (mean 28.4 mg/l) and ESR (mean 36.3 mm/h). IBD were diagnosed in 9 (22.5 %) cases: 5 (12.5 %) patients with Crohn's disease and 4 (10 %) patients with ulcerative colitis, in the remaining (77.5 %) cases there was no intestinal pathology.Conclusion. The results showed high frequency of IBD in patients with AS. Patients with high fecal calprotectin levels (more than 100 μg/g) had high disease activity (AS). In most cases, inflammatory bowel disease were diagnosed in patients AS with fecal calprotectin levels more than 100 µg/g.

BackgroundCurrently, there is a lot of interest in the frequency and risks of developing of inflammatory bowel diseases (IBD) in patients with ankylosing spondylitis (AS) [1]. IL-17 and IL-23 are one of the key pathogenetic markers of AS [2]. A lot of studies also showed that the average number of IL-17 cells was significantly increased in active Ulcerative colitis (UC) and Crohn disease (CD) patients [3]. According to some studies cytokines, such as IL-17 and IL-23, play crucial role in intestinal protection and homeostasis [4].ObjectivesThe aim of this study was to evaluate IL-17 and IL-23 serum levels in patients with AS without IBD and with AS and IBD.MethodsIn the analysis were included 50 patients with AS, fulfilling the modified New York criteria, among them man-36 (72%), woman-14 (28%), mean age of patients was 42.5±9.9, mean disease duration – 13.4±8.7 years. All patients were examined with ESR, CRP, esophagogastroduodenoscopy, colonoscopy, IL-17 and IL-23, using enzyme-linked immunosorbent assay for the quantitative measurement of IL-17 and IL-23 in serum ELISA kit. IL-17 and IL-23 levels were also studied in control group (13 healthy donors), mean IL-17 was 1.16±1.02 pg/mL, mean IL-23 was 33.03±18.02 pg/mL.ResultsAll patients had a high disease activity, mean BASDAI was 5.3± 1.8, mean ASDAS CRP 3.7±1.01, mean ASDAS ESR 3.6±1.01. IBD were diagnosed in 11 cases: 6 patients (12%) with CD and 5 patients (10%) - UC, in the remaining cases (78%-39 patients) was no intestinal pathology. Patiens with AS had higher levels of IL-17(10.4±9.1 pg/ml) and IL-23(188±156 pg/ml), than the group of healthy donors. Patients with AS and IBD had slightly lower IL-17(6.7±4.5 pg/ml) and IL-23(155.5±97 pg/ml) levels than patients with AS without IBD(p=0.03). IL-23 was positively correlated with ESR (r=0.5) and CRP (r=0.5) (p <0.001) levels, however IL-17 level had negative correlation with ESR and CRP level (r=-0.2) (p<0.001).ConclusionIL-23 and IL 17 serum levels in patients with AS and IBD was lower than in patients with AS without IBD. There is a significant association between the CRP, ESR and IL-23 level, but not with IL-17.References[1]Lukina G.V., Kulakova P.I., Novikov A.A., Savenkova N.A., Alexandrova E.A., Volnukhin E.V., Kovshik A.N. Frequency of inflammatory bowel diseases in patients with ankylosing spondylitis. Medical alphabet. 2019;2(37):12-15. https://doi.org/10.33667/2078-5631-2019-2-37(412)-12-15.[2]Sherlock JP, Taylor PC, Buckley CD. The biology of IL-23 and IL-17 and their therapeutic targeting in rheumatic diseases. Curr Opin Rheumatol. 2015 Jan;27(1):71-5.doi:10.1097/BOR.0000000000000132.[3]Fujino S, Andoh A, Bamba S, et al. Increased expression of interleukin 17 in inflammatory bowel diseases. Gut.2003;52:65-70.[4]Shen W, Durum SK. Synergy of IL-23 and Th17 cytokines: new light on inflammatory bowel disease. Neurochem Res. 2010 Jun;35(6):940-6. doi: 10.1007/s11064-009-0091-9Disclosure of InterestsNone declared

BackgroundAnkylosing spondylitis (AS) is an immune-mediated inflammatory disease of the musculoskeletal system, that is often accompanied with a subclinical intestinal inflammation. Inflammatory bowel diseases (IBD), including, Crohn’s disease (CD) and ulcerative colitis (UC), are the most frequent extra-articular manifestation in patients (pts) with AS. Several autoantibodies and antimicrobial antibodies are used as additional non-invasive serological markers for the diagnosis of CD and UC [1]. The evaluation of IBD-associated antibodies in AS pts provided conflicting results [2, 3].ObjectivesThe aim of the study was to determine the serum levels of IBD-specific antibodies in AS.MethodsWe studied 51 pts with AS fulfilled modified New York criteria (1984); (40M/11F); median and interquartile range (25th—75th percentile) of age 44.0; 34.0-49.0 years; disease duration 12.0; 5.0-20.0 years; BASDAI - 5.3; 4.5-6.4; ASDAS ESR - 3.6; 3.0-4.4; ASDAS CRP - 3.7; 2.8-4.5; 40% HLA-27 positive. In 22% of pts with AS, IBD (CD and UC) were diagnosed. The control group included 44 healthy donors (HC). Atypical perinuclear anti-neutrophil cytoplasmic antibodies (pANCA) were detected using indirect immunofluorescence. The serum levels of IgA/IgG antibodies to Saccharomyces cerevisiae (ASCA), IgA/IgG antibodies to glycoprotein 2 (GP2), IgG antibodies to cathepsin G, lactoferrin, elastase and bactericidal permeability-increasing protein (BPI) were detected by ELISA.ResultsAS pts without signs of IBD and AS with IBD (AS/IBD) pts had significantly higher serum levels of IgA ASCA, IgA anti-GP2, anti-elastase antibodies than HC (4.5; 2.6-6.4 U/ml and 4.9; 3.7-7.3 U/ml vs 1.9; 0.6-2.6 U/ml, p=0.0008, p=0.001; 1.2; 0.8-5.5 U/ml and 1.2; 0.9-11.8 U/ml vs 0.7; 0.6-1.3 U/ml, p=0.007, p=0.02; 8.2; 5.9-9.9 U/ml and 9.1; 8.5-10.5 U/ml vs 5.6; 4.7-8.3 U/ml, p=0.01, p=0.003). The median concentration of anti-cathepsin G antibodies was greater for AS/IBD pts than AS pts (0.8; 0.5-1.0 U/ml vs 0.4; 0.3-0.6 U/ml, p=0.02). In AS and AS/IBD, the occurrence of anti-elastase antibodies (23.0%, 33.0%) was higher than for HC (0%, p=0.05, p=0.01). The positivity rate of IgA anti-GP2 in AS/IBD exceeded that in HC (27.0% vs 0%, p=0.025). AS/IBD pts demonstrated a higher prevalence of pANCA (36.0%), and anti-BPI antibodies (36.0%), when compared to AS alone (4.8%, p=0.005, and 8.0%, p=0.02) and HC (0%, p=0.0001, and 0%, p=0.008).ConclusionOur findings indicate that elevated serum levels of IgA ASCA, IgA anti-GP2, anti-elastase antibodies in AS did not differ from those in AS/IBD and may serve as potential biomarkers for predicting intestinal inflammation at an early stage. For AS/IBD, the most useful diagnostic markers were atypical pANCA, IgA ASCA, IgA anti-GP2, anti-elastase and anti-BPI antibodies.References[1]Prideaux L, De Cruz P, Ng SC, Kamm MA. Serological antibodies in inflammatory bowel disease: a systematic review. Inflamm Bowel Dis. 2012; 18(7):1340-55.[2]Benfaremo D, Luchetti M, Gabrielli A. Biomarkers in inflammatory bowel disease-associated spondyloarthritis: state of the art and unmet needs. J Immunol Res. 2019 May 30; 2019:8630871.[3]De Vries M, Van Der Horst-Bruinsma I, Van Hoogstraten I., et al. pANCA, ASCA, and OmpC antibodies in patients with ankylosing spondylitis without inflammatory bowel disease. J Rheumatol. 2010; 37(11):2340–4.Disclosure of InterestsNone declared